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Laboratory Animal Medicine Blue Book, 3rd Ed. (2015) > Chapter 14. Biology and Diseases of Ferrets > Flashcards

Chapter 14. Biology and Diseases of Ferrets Flashcards

1
Q

Ferret taxonomy

A

Family Mustelidae
Subfamily Mustelinae
Genus Mustela
Mustela putorius furo

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2
Q

Subfamily Mustelinae

A

Includes weasels, mink, ferrets (genus Mustela), martens (genus Martes)

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3
Q

Genus Mustela

A

5 subgenera: Mustela (weasels), Lutreola (European mink), Vison (American mink), Putorius (ferrets) Grammogale (South American weasels)

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4
Q

Family Mustelidae

A
  • Smallest member = least weasel (Mustela nivalis)

- Largest member = sea otter (Enhydra lutris)

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5
Q

Ferret use in research

A
  • Influenza pathogenesis
  • Virology
  • Neuroscience
  • Carcinogenesis
  • Cardiovascular physiology
  • Emesis
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6
Q

Sources of ferrets

A
  • Large-scale commercial production (available in US) - inbreeding related to disease susceptibility?
  • Fur operations
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7
Q

Commercials stocks of ferrets

A

-Based on coat color: albino, sable (‘fitch’, ‘wild’; most common), Siamese, silver mitt, Siamese-silver mitt (Siamese with white chest and feet)

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8
Q

US ferrets with blaze or white head

A
  • Up to 75% can have Waardenburg syndrome & are deaf
  • Physiologic basis: ipsilateral projections of the cochlear nucleus to the auditory midbrain in albino ferrets
  • Albino ferrets also have impaired motion perception & contrast sensitivity
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9
Q

Recommended temperature ranges for ferrets

A
  • Tolerate low temps well & high temps poorly
  • Juveniles & adults: 4-18 C (39.2-64.4 F)
  • <6 weeks old: greater than 15 C; kits under this age require a heat source if separated from dam; older group-housed kits do not
  • Elevated temps (>30 C; 86 F) cannot be tolerated by ferrets
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10
Q

Why can’t ferrets tolerate high temperatures?

A

Poorly developed sweat glands = susceptible to heat prostration
-Signs of heat stroke: panting, flaccidity, vomiting

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11
Q

Recommended humidity range for ferrets

A

40-65%

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12
Q

Recommended lighting for ferrets

A
  • 12:12 dark-light appropriate for non-breeding animals housed for <6 months
  • 16 hr light daily for breeding and lactating jills
  • Ferrets maintained beyond 6 mths should be exposed to a ‘winter’ = 6 weeks per year of 14 hr dark daily to maintain physiologic normalcy
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13
Q

Light cycle for time-pregnant jills

A

Maintain light cycle that time-pregnant jills were exposed to prior to shipment; failure to do so can results in negative energy balance & pregnancy toxemia

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14
Q

Recommended air changes for ferret housing

A
  • 10-15 air changes per hour
  • Use nonrecirculated air b/c of strong ferret odor & susceptibility of ferrets to human respiratory tract infections
  • Ferret odor should not overlap any rodent housing areas b/c rodents have instinctive fear of ferrets; scent can disrupt rodent breeding and physiology
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15
Q

Social housing of ferrets

A
  • Females can be housed singly or in groups
  • Estrous females that are cohoused may become pseudopregnant
  • Intact males should be housed individually after 12 weeks of age
  • Weanling ferrets (4- 12 week old) may be group housed
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16
Q

Spacing of grid wall for ferret caging

A

1 x 0.5 inches apart, or 0.25 inch if using wire mesh

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17
Q

Potentional health concerns for ferret caging

A
  • Zinc toxicosis reported in ferrets licking galvanized bars from which metals had leached during steam sterilization
  • Clay litters can cause chronic upper resp infx due to inhaled dust
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18
Q

Cage size for ferrets

A

24x24x18 inches = adequate for 2 adults

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19
Q

Diet parameters for ferrets

A
  • Protein source: meat
  • Nonbreeding adults = 18-20% fat, 30-40% protein
  • Breeding adults = 25% fat, minimum 35% protein
  • Peak lactation = minimum 30% fat, minimum 35% protein
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20
Q

Food and water consumption of ferrets

A
  • Feed ad libitum
  • Food: 43 g/kg body weight
  • Water: 75-100 mL daily
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21
Q

Enrichment for ferrets

A
  • Sleeping locations: snooze tube, hammock, PCV pipe or dryer hose
  • Digging behavior: box filled with rice, plastic balls, crumpled paper balls
  • Enrichment lowers fecal glucocorticoid metabolites (FGM) in juvenile males; this study also showed juvenile males interacted with enrichment more than juvenile females (no effect on juvenile female FGM)
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22
Q

Unique anatomy of ferrets - thorax

A
  • Thorax is narrow & elongated with proportionally long trachea = good for studies of tracheal physiology
  • Tracheal size & laryngeal anatomy make intubation somewhat challenging = ferrets used for pediatric intubation training
  • Lung relatively large; total lung capacity is nearly 3x what would be predicted based on body size compared to other mammals = pulmonary research model
  • Higher degree of bronciolar branching with more extensive bronchial submucosal gland compared to dog = pulmonary research model
  • Paired common carotid arteries arise from the brachiocephalic trunk at the level of the thoracic inlet (like dogs & cats)
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23
Q

Unique anatomy/physiology of ferrets - abdomen

A
  • Carnivore = simple monogastric stomach
  • NO cecum; indistinct ileocecal transition makes it difficult to identify junction of small and large intestines grossly
  • Length of alimentary tract is very short relative to body size = GI transit time as short as 3 hr
  • Extramedullary hematopoiesis common in spleen; can result in splenomegaly
  • Ferrets have no naturally occurring antibodies against unmatched erythrocyte antigens & none develop even with repeated transfusions
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24
Q

Scent glands of ferrets

A
  • Paired anal scent glands; well-developed
  • Animals can be descented surgically
  • Some animals, especially intact males & estrous jills, may still have musky odor even after descenting because of normal sebaceous secretions
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25
Q

Sweat glands of ferrets

A

-Ferrets lack well-developed sweat glands = predisposed to prostration when ambient temps reach 32 C (90 F)

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26
Q

Unique anatomy/physiology of ferrets - reproductive

A
  • Seasonal breeders
  • Prolonged estrus in unbred females can result in aplastic anemia - can reproduce this with exogenous estrogen administration
  • Males has os penis & prostate gland
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27
Q

Ferret weight ranges

A
  • Newborn kits: 6-12 g at birth
  • 6-8 weeks: 400 g
  • Intact males: 1-2 kg
  • Intact females: 0.5-1 kg
  • Gonadectomized adults: 0.8-1.2 kg
  • Body weight can fluctuate up to 30-40% with seasonal changes
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28
Q

Ferret lifespan

A

6-8 years; rarely up to 11 years

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29
Q

Normal body temperature for ferrets

A

38.8 C (37.8-40 C)

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30
Q

Chromosome number for ferrets

A

40 (diploid)

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31
Q

Dental formula for ferrets

A

2 (I 3/3, C 1/1, P 4/3, M 1/2)

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32
Q

Vertebral formula for ferrets

A

C7-T15-L5-S3-C14

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33
Q

Age of sexual maturity for ferrets

A

4-12 months

-Length of breeding life is 2-5 years

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34
Q

Gestation length in ferrets

A

42 +/- 2 days

-Litter size 1-18, average 8

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35
Q

Kit development in ferrets

A
  • Birth weight: 6-12 g
  • Eyes open: 34 days
  • Onset of hearing: 32 days
  • Weaning: 6-8 weeks
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36
Q

Erythron in ferrets

A

-Ferrets have relatively robust erythron, with Hct, Hbg, and total RBC & reticulocyte counts generally higher than dog or cat

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37
Q

Proteinuria in ferrets

A
  • A low grade proteinuria on UA may be seen in normal, healthy ferrets
  • Normal USG in intact males: 1.051, intact females: 1.042
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38
Q

Ferret nutrition

A
  • Strict carnivores
  • Short GI tract & rapid GI transit time require protein to be readily digestible
  • Daily maintenance energy requirement: 0.5 MJ metabolizable energy (ME)/kg metabolic body weight (BW^0.75)
  • In MINK: 42% protein up to 16 weeks; after 16 weeks old, 26-36% protein, 9-28% fat, 22-42% carbohydrate
  • 30-40% protein & 18-20% fat for adults; minimum 35% protein & 25% fat for reproductively active & growing animals
  • Diets high in fish or with raw meat not recommended
  • Digestibility of crude protein in ferrets significantly lower than cats & digestibility of crude fat significantly higher = ferrets cannot be used as a model of cats & careful comparing data between two species
  • Carbohydrates should not exceed 30-36% for adults, but kits feed carb-free diet reported to do poorly d/t hypoglycemia
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39
Q

High levels of plant protein in ferret diets

A

Can lead to urolithiasis

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40
Q

Ferrets in Beta-carotene research

A
  • Used to investigate absorption, metabolism, interaction of Beta-carotene & Vit E
  • Ferrets, like humans, convert Beta-carotene to Vit A in the gut & absorb Beta-carotene intact
  • Beta-carotene, retinol & retinyl esters are absorbed intact into the lymph & cleavage products (Beta-apo-12’-carotenal, Beta-apo-10’-carotenal, retinoids) accumulate in intestinal mucosa - mucosa converts Beta-carotene into retinoic acid - transported via portal vein to liver
  • Beta-carotene absorption & conversion into retinol enhanced by coperfusion of alpha-tocopherol
  • Ferrets able to excrete retinol & retinyl esters into urine - depends on oral Vit A supplementaton
  • Lung cancer model of ferrets exposed to tobacco smoke has been used to evaluate the cancer-modulating properties of these micronutrients
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41
Q

Ferret water consumption

A
  • 75-100 mL per day, depending on dry matter content of feed

- Provide fresh water ad libitum in secured bowels or water bottles (ferrets will overturn is not well secured)

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42
Q

Ferret reproductive calendar

A
  • Seasonal breeders

- In the wild, season in Northern Hemisphere is March-August for females & December-July for males

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43
Q

Estrous cycle in ferrets

A
  • -Puberty: 6-12 months
  • Minimum breeding age: 8-12 mths male, 4-5 mths female
  • Monestrous, continuous duration until intromission
  • Induced ovulators
  • Jills maintained at 8 hr light-16 hr dark reach puberty in 10-12 months
  • The transfer from short to long photoperiods should not occur prior to 90 days of age, b/c jills that are prematurely transferred will remain anestrous
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44
Q

Gestation period in ferrets

A

42 +/- 1 day

-Average litter size 8 (1-18)

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45
Q

Estrus in ferrets

A
  • Vulvar swelling is hallmark sign
  • NOT assoc w/ rising FSH like in rodents
  • Mated ~14 days after vulvar enlargement
  • Estradiol concentrations responsible for development of female reproductive tract & secondary sexual characteristics
  • Tonic inhibition of LH secretion by the anterior pituitary during both prepubertal life and anestrus
  • With increasing light exposure, LH levels rise despite estradiol
  • Jills may return to estrus during 2nd-3rd week of lactation if they have fewer than 5 kits, or 2 weeks after weaning if litter is larger
  • Jills should be rebred or given hCG to terminate estrus, even if still lactating
  • May have 2-3 litters yearly until 5 years old
  • A nonstimulatory photoperiod should be used 6 weeks per year to rest the ferret and preserve maximum fertility - jills return to estrus ~3 wks after reinstitution of longer photoperiod
  • Return of estrus correlates with follicular development and increased plasma estradiol
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46
Q

Reproductive physiology of male ferrets

A

-Age differences in the sensitivity of negative feedback inhibition of the hypothalamic secretion of gonadotropin-releasting hormone (GnRH) by testosterone, or to estrogenic compounds derived from aromatization of testosterone, appear to be essential in determining puberty & seasonality of reproduction in males

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47
Q

Ovulation in ferrets

A

5-13 ova ovulated 30-40 hr after coitus = induced ovulators

  • Neck restraint and intromission by the male required for ovulation
  • Implantation occurs 12 days after mating
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48
Q

Placentation of ferrets

A

-Zonary & endotheliochorial (typical for carnivores)

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49
Q

Pregnancy detection in ferrets

A
  • Ultrasound detection as early as day 12
  • Palpation as early as day 14
  • Calcified fetal skeletons on radiographs at ~30 days
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50
Q

Husbandry needs of pregnancy ferrets

A
  • Separate to single housing when within 2 weeks of parturition
  • Provide nest box with bedding for warmth
  • Next box should be at least 6 inches deep
  • Nutritional support very important: risk for pregnancy toxemia = hypoglycemia, hyperketonemia, hypoinsulinemia, decreased T4 & T3, hepatic lipidosis
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51
Q

Parturition in ferrets

A
  • Rapid, as little as 2-3 hr
  • Primiparous jills usually deliver on day 41, multiparous on day 42
  • Fetuses remaining in utero beyond day 43 typically die
  • Dystocia is common d/t positional abnormalities and fetal oversize = C-section; failure to deliver within 8 hr after administration of prostaglandin is indication for C-section
  • Leave undisturbed for several days postpartum to minimize cannibalization
  • Fostering: allow pups to mingle with foster jill’s own pups while jill is away so that rejection d/t olfactory stimuli will not occur
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52
Q

Development of newborn ferrets

A
  • Born altricial; dependent on jill for first 3 weeks
  • Coat color starts to become visible at 3 days of age
  • Weigh 6-12 g at birth
  • Sexual dimorphism in size apparent by week 7
  • Eruption of deciduous teeth = 14 days
  • Ability to hear = 32 days - ear canals do not open until 32 days - startle response in kits
  • Opening of eyes = 34 days
  • Eruption of permanent canines = 47-52 days
  • Displacement of deciduous canines by 56-70 days
  • POLECATS = learn scent of prey between 60-90 days
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53
Q

Weaning in ferrets

A
  • 6 weeks of age
  • Can give slurry of adult food with fat supplementation to achieve 30% fat (Linatone supplement)
  • Diet should be 30% fat, 40% protein
  • Group housed until sexually mature
  • Males >12 weeks old may fight if exposed to greater than 12 hr of light per day
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54
Q

Clostridium perfringens Type A - etiology, transmission

A
  • Etiology: Clostridium perfringens Type A
  • Ubiquitous, present in GI tracts of humans & animals
  • Acute abdominal distenstion, dyspnea, cyanosis in weanling ferrets
  • Predisposing factors: overeating, sudden changes in diet, proliferation of C. perfringens type A & its toxins
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55
Q

Toxins of Clostridium perfringens Type A

A

-Alpha toxin: principal lethal toxin; hemolytic and necrotizing & has ability to split lecithin or lecithin-protein complexes, leading to destruction of cell membranes & necrosis

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56
Q

Clostridium perfringens Type A - clin signs, diagnosis

A
  • Clin signs: acute abdominal distension, cyanosis, found dead & bloated
  • Diagnosis: isolation of bacteria from stomach/intestines; toxin identification using mouse protection assay
  • Necropsy findings: markedly distended stomach & intestines with large amount of gas & brown semiliquid ingesta; SC emphysema
  • Histo: abundant G(+) bacilli in smears of gastric and intestinal contents; GI mucosa necrosis, G(+) baclli lining denuded mucosal surface & extending into gastric glands, intestinal crypts; lymphoid necrosis of LNs, spleen, thymus; mild to moderate dilation of central hepatic sinusoids with hepatocellular dissociation and multifocal aggregates of necrotic neutrophils within portal areas
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57
Q

Clostridium perfringens Type A - treatment, control

A
  • Prevention: good management & feeding practices; restrict feeding of weanlings to 2x instead of 3x daily
  • Tx: supportive care, gastric trocharization - these can be unrewarding
58
Q

Campylobacteriosis - etiology, transmission

A
  • Etiology: Campylobacter jejuni; G(-) spirally curved microaerophilic bacteria
  • Causes diarrheic illness in humans, dogs, cats, cows, goats, pigs, mink, ferrets, sheep; mastitis in cows, infectious hepatitis in chickens; abortion in cattle, sheep, goats, dogs, mink
  • Can be cultured from asymptomatic dogs, cats, ferrets
  • Transmission: ingestion of organisms through direct contact with feces or contaminated feed & water
59
Q

Campylobacteriosis - clin signs, diagnosis

A
  • Clin signs: self limiting diarrhea; anorexia, dehydration, tenesmus; fetal resorption, abortion
  • Diagnosis: based on history, clinical signs, culture - grows slowly & need selective media or filtration techniques w/ temp 42-43 C & microaerophilic conditions; round, raised, translucent & sometimes mucoid colonies
  • Ddx: proliferative bowel disease, other infectious and noninfectious causes of diarrhea
60
Q

Campybacteriosis - pathology, treatment, control

A
  • Necropsy findings: neutrophilic infiltrates in lamina propria of colon; enterocolitis; placentitis
  • Tx: supportive care, antibiotics based on C&S; azithromycin & fluoroquinolones commonly used in humans; experimental killed whole cell vaccine protected 80% of ferrets when given 4 doses 48 hr apart
  • Control: ZOONOTIC = isolate positive animals; good hygiene
61
Q

Helicobacter mustelae - etiology, transmission

A
  • Isolated from margins of a duodenal ulcer of a ferret
  • Every ferret with chronic gastritis is infected with H. mustelae; SPF ferrets do not have gastritis, gastric ulcers, or detctable IgG antibody
  • Robust model for H. pylori gastritis in humans
  • Colonizes nearly 100% of ferrets shortly after weaning; may be due to fecal-oral transmission
  • Ferrets placed on proton pump inhibitors, which raise gastric pH, have a statistically higher recovery of H. mustelae from feces when compared with age-matched untreated control ferrets
  • Ferret is ONLY domesticated animal to date with naturally occurring helicobacter associated ulcer disease
62
Q

Helicobacter mustelae - clin signs, diagnosis

A
  • Clin signs: gastric or duodenal ulcers - vomiting, melena, chronic weight loss, lowered hematocrit; gastric adenocarcinoma - vomiting, anorexia, weight loss
  • Ddx: gastric foreign body
  • Dx: endoscopy; gastric samples inoculated onto blood agar plates supplemented with trimethoprim, vancomycin, polymixin B - incubate at 37 or 42 C in a microaerobic atmosphere for 3-7 days; H. mustelae = produce urease, catalase, oxidase; resistant to cephalothin; sensitive to nalidixic acid
63
Q

Helicobacter mustelae - pathology, treatment, control

A
  • Superficial gastritis with H. mustelae on surface of mucosa but NOT in crypts; diffuse antral gastritis; focal glandalar atrophy (a precancerous lesion) & regeneration; can see deep colonization focally in antrum
  • Argyrophilic bacteria in liver, biliary tract - chronic cholangiohepatitis, bile duct hyperplasia, cholangiocellular carcinoma (H. cholecystus)
  • Susceptible to gastric cancer = gastric adenocarcinoma, gastric mucosa associated lymphoid tissue (MALT) lymphoma
64
Q

Helicbacter mustelae - treatment, control

A
  • Tx: triple therapy with amoxicillin, metronidazol, bismuth subsalicylate 3x daily for 3-4 weeks; ranitidine bismuth & clarithromycin 3x daily for 2 weeks
  • Eradicaton associated with decrease in anti-H. mustelae IgG antibody titers (consistent with findings in humans)
  • Omeprazole induces hypochlorhydria & may be used in conjunction with antibiotics to treat H. mustelae-assoc duoenal or gastric ulcers; cimetidine can also be used to decrease acid secretion; sucralfate for clinical signs of stomach ulcers
  • Fluids & blood transfusions for acute bleeding ulcers
65
Q

Proliferative bowel disease in ferrets - etiology, transmission

A
  • Etiology: Lawsonia intracellularis = intracellular Campylobacter-like organisms related to Desulfovibrio spp.; G(-), comma to spiral-shaped bacteria
  • Transmission: fecal-oral
  • Disease of young ferrets
  • Copathogens include Campylobacter spp, coccidia, chlamydia
66
Q

Proliferative bowel disease - clin signs, diagnosis

A
  • Clin signs: chronic diarrhea, lethargy, anorexia, weight loss, dehydration; diarrhea may be blood-tinged, contain mucus, often green in color; rectal prolapse; ataxia and muscle tremors
  • Dx: clinical signs, palpably thickened colon, colonic biopsy
  • Ddx: other causes of diarrhea and weight loss
67
Q

Proliferative bowel disease - pathology, differentials, treatment

A
  • Segmented, thickened large bowel - usually terminal colon, can also include ileum and rectum
  • Histo: marked mucosal proliferation and intracytoplasmic L. intracellularis seen with silver stain in apical portion of epithelial cells; mixed inflammatory infiltrate; reduced goblet cell production; hyperplasia of glandular epithelium; glandular irregularity with penetration of mucosal glands through the muscularis mucosa; increased thickness of tunica muscularis
  • Translocation of glandular tissue to extraintestinal sites - regional LNs & liver - has been reported
  • Ddx: other causes of diarrhea and wasting, including dietary changes, eosinophilic gastroenteritis, gastric foreign body, lymphoma, Aleutian disease (AD), gastric ulcers
  • Incidence appears to be rare
  • Tx: supportive care; chloramphenicol or metronidazole for 2 weeks
68
Q

Tuberculosis in ferrets - etiology, transmission

A
  • Etiology: Mycobacterium bovis, M. avium, M. tuberculosis
  • Aerobic, G(+), non-branching, non-spore-forming, acid-fast rods
  • Ferrets might be more susceptible to mycobacterial infections than other species; can have natural infections with M. bovis and M. avium; also susceptible to experimental infx with human tubercle bacillus; endemic in feral ferrets inf New Zealand
  • Feeding of commercial diets and TB testing in livestock and poultry has reduced incidence of the disease in ferrets
  • Horizontal transmission demonstrated in ferrets under experimental housing conditions
  • Den sharing, playing, fighting, sniffing, cannibalism, and aggressive breeding could transmit TB between ferrets
  • M. celatum infx reported in one ferret - accurate dx difficult because reacts positively with polyclonal Abs against M. paratuberculosis & M. bovis = identify using 16S rRNA sequence analysis
69
Q

Tuberculosis in ferrets - clin signs, pathology

A
  • M. bovis causes typical microscopic foci of infection & necrosis; M. avium may not cause these in all ferrets; human TB causes just localized infx with minor spread to adjacent LNs
  • Weight loss, anorexia, lethargy, death, miliary lesions of lungs & other viscera, progressive paralysis
  • Mesenteric LNs often infected - related to ORAL infection
  • Histo: granulomatous inflamm w/ predominantly macrophages, multnucleated giant cells, epithelioid cells - in lungs, intestines, spleen, liver, peripancreatic adipose tissu; numerous acid-fast bacilli within macrophages
  • Impaired cell-mediated response may account for the large number of organisms observed in M. bovis lesions
70
Q

Tuberculosis in ferrets - diagnosis, treatment, control

A
  • Dx: isolation of organism in tissue; most common sites = retropharyngeal & mesenteric LNs
  • A tuberculin skin testing regimen has NOT been definitively characterized for ferrets yet
  • Tx: euthanasia b/c ZOONOTIC; clarithromycin, rifampicin, clofazimine
71
Q

Salmonellosis in ferrets - etiology, transmission

A
  • G(-), non spore forming, facultative anaerobic rods in family Enterobacteriaceae
  • Genus Salmonella has 2 species: S. bongori = poikilotherms & rarely humans, S. enterica
  • Transmission: ingestion from contaminated food or water products
  • Serotypes that have been isolated from ferrets include S. Hadar, S. Enteritidis, S. Kentucky, S. Typhimurium
72
Q

Salmonellosis in ferrets - clin signs, pathology

A
  • Conjunctivitis, rapid weight loss, tarry stools, febrile, lethargy, anorexia, trembling, abortion/stillbirth
  • Gross lesions: tissue pallor, petechiae of gastric mucosa, melena, dark fibrinous exudate in large intestine, GI contents containing lots of mucus, some blood
  • Histo: desquamated epithelium of GI mucosa, exudate in small intestine containing mucoid material, RBCs, desquamated intestinal villi; edematous villi in ileum, infiltration of small intestinal mucosa with lymphocytes and macrophages; necrotic foci in liver, spleen, kidney; splenomegaly, visceral lymphadenopathy; necrotizing endometritis
73
Q

Salmonellosis in ferrets - diagnosis, treatment, control

A
  • Dx: based on history, clinical signs, isolation of organism - culture on enrichment and selective media
  • Tx: sulfathalidine in feed; supportive care; antibiotics based on C&S
74
Q

Pneumonia in ferrets

A
  • Streptococcus zooepidemicus & other group C & G streptococci; Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bordetella bronchiseptica
  • Primary bacterial pneumonia not very common; may occur secondary to megaesophagus in ferrets, or secondary to influenza
  • EXCEPTION: outbreak of Mycoplasma species in ferrets as primary pathogen
  • Clin signs: nasal discharge, dyspnea, lethargy, anorexia, increased lung sounds, cyanosis, fever, sepsis, death
  • Dx: history, clin signs, CBC, culture and cytology of tracheal or lung wash, radiographs
  • Ddx: dilated cardiomypathy, heartworm, mycotic pneumonia, pneumocystis pneumonia in immunosuppressed animals, neoplasia, influenza
  • Tx: antibiotics, supportive care, oxygen
75
Q

Abscesses in ferrets

A
  • Staphylococcus spp, Streptococcus spp, Corynebacterium spp, Pasteurella, Actinomyces, hemolytic E. coli, Aeromonas spp
  • Of lung, liver, uterus, vulva, skin, mammary glands, oral cavity
  • May result from wounds inflicted by biting during fighting, playing, mating, chewing sharp objects
  • Clin signs: localized swellings +/- draining tracts - usually SC abscesses are walled off & don’t cause systemic signs; may see dental abscesses d/t canine tooth fracture; stranguria d/t prostatic abscessation - often secondary to hyperadrenocorticism
  • Dx: cytology & Gram staining of aspirate
  • Ddx: myiasis, granuloma, hematoma, neoplasia
  • Tx: prevent exposure to sharp objects, limit exposure of male and female during breeding, antibiotics & establish drainage
76
Q

Mastitis in ferrets - etiology, transmission

A
  • G(+) cocci like Streptococcus spp, Staphylococcus aureus & coliforms like hemolytic E. coli most frequently associated
  • Factors that may be involved: stress of lactation, injury to mammary glands by kits, environmental contamination, virulence of the organism
  • Organism may be present in oral cavity of kits
77
Q

Mastitis in ferrets - clin signs, diagnosis

A
  • Acute form: occurs soon after parturition or after 3rd week of lactation - glands are swollen, firm, red or purple, painful, may become gangrenous
  • Chronic form: may occur when kits are 3 weeks old or as sequela to acute form = glands that are firm but NOT painful or discolored
  • Dx: history, clin signs, PE findings, isolation of organism
  • E. coli often positive for cnf1 = tend to produce extraintestinal disease & are referred to as necrotoxigenic E. coli
78
Q

Mastitis in ferrets - pathology, treatment

A
  • Glands swollen, overlying skin discolored
  • Edema, hemorrhage, coagulative & liquefactive necrosis of glandular tissue & surrounding SC tissue
  • Mixed leukocytic infiltrate - primarily PMN leukocytes, large numbers of bacteria, thombosis and necrosis of vessels
  • Tx: broad-spectrum antibiotics; recommend oral administration of antibiotics to nursing kits also; surgical resection & debridement may be needed for acute mastitis; kits may spread infection to foster jills!; good hygiene to minimize spread to other jills; euthanisia for chronic mastitis
79
Q

Canine distemper in ferrets

A
  • Paramyxovirus; genus Morbillivirus (related to measles, rinderpest)
  • Several strains, including a ferret adapted strain
  • Virus can be inactivated by heat, light, phenol, Roccal, sodium hydroxide, formalin
  • Most serious viral infection of ferrets; mortality up to 100%
  • Catarrhal Phase: 7-10 days postinfx; anorexia, pyrexia, photosensitivity, serous nasal discharge, erythematus pruritic rash (cell-mediated immunity to infected endothelial cells), hyperkeratosis of footpads (not always seen); secondary bacterial - mucopurulent ocular and nasal discharge, pneumonia
  • CNS Phase: ataxia, tremors, paralysis; may or may not be preceded by catarrhal phase
  • Death in 12-16 days from ferret strains, up to 35 days from canine strains
80
Q

Canine distemper in ferrets - transmission, epizootiology

A
  • Virus shed in conjunctival, nasal, oral exudates, urine, feces, sloughed skin
  • Ferrets very susceptible to infection via respiratory route
  • Viremia detectable 2 days postinfection & persists until ferret mounts a neutralizing antibody response
  • Primary site of replication = respiratory and lymphatic systems
  • Decrease in lymphocyte subsets at 5-30 days postinfection
  • Moves to CNS via infection of vascular endothelial cells and hematogenous spread of virus infected leukocytes from meningeal blood vessels into the subarachnoid space = widespread infection of cells of pia and arachnoid mater of the leptomeninges over large areas of the cerebral hemispheres
81
Q

Canine distemper in ferrets - clin signs, diagnosis

A
  • Intracytoplasmic & intranuclear inclusion bodies in tracheal, bronchial epithelia; bile duct; transitional epithelium of bladder
  • Inclusions = eosinophilic (H&E) inclusions, appear orange using Pollack’s trichrome stain
  • Dx: fluorescent antibody test on peripheral blood & conjunctival mononuclear cells; RT-PCR; cytology of conjunctival scrapings
  • Ddx: Bordetella bronchiseptica, influenza (does not rapidly progress to mucopurulent ocular and nasal discharge like CD)
82
Q

Canine distemper in ferrets - treatment, control

A
  • Isolate clinically affected ferrets; euthanasia recommended as no reports of animals surviving acute infection
  • Vaccination can prevent infx: MLV of chicken embryo tissue culture origin (CETCO) given IM
  • Vaccinate kits every 2-3 weeks from 6 weeks old to 14 weeks, then annually
  • Vaccine reactions have been reported following double-dose vaccination (follow schedule above) - vomiting, diarrhea, fever, collapse
  • Treat vaccine reaction with diphenhydramine IV or IM or epinephrine SC, IV, IM, intratracheal
  • Inactivated vaccines do not deliver consistent effective immunity = NOT recommended
  • CD used to experimentally study mobillivirus infection and vaccine strategies in humans
83
Q

Experimental infection of ferrets with viruses

A
  • Feline panleukopenia, canine parvovirus, canine parainfluenza, mink enteritis virus, respiratory syncytial virus, transmissible mink encephalopathy, pseudorabies
  • Natural infection with these viruses has not been reported
84
Q

Aleutian disease - etiology, transmission

A
  • Aleutian mink disease virus (ADV) = parvovirus in genus Amdoparvovirus, species Carnivore amdoparvovirus 1
  • Most common strain = ADV-F
  • Mink derived strains more virulent to mink than ferrets; at least 3 strains that are distinct from the mink ADV have been documented in ferrets
  • Hypergammaglobulinemia (HGG) = immunomodulation that is disruptive to research
  • Transmission: direct or via aerosol of urine, saliva, blood, feces, fomites; vertical transmission established in mink but unproven in ferrets
85
Q

Aleutian disease - clin signs, diagnosis

A
  • Ferrets infected as adults = persistent infection but rarely disease; chronic progressive weight loss, cachexia, malaise, melena
  • May cause ataxia, paralysis, tremors, convulsions
  • Lesions typically immune-mediated; elevation of gammaglobulins >20% of the total proteins; in mink there is depression of B & T cell responses
  • Dx: HGG and chronic weight loss; IFA or counter-immunoelectrophoresis (CIEP) for antibody to ADV antigen; ELISA & PCR
  • Presence of ADV antibody in a ferret is NOT necessarily diagnostic of the disease in an animal (up to 10% of ferrets may be antibody positive without disease)
  • DNA of ADV can be detected by in situ hydrixization - can use on paraffin embedded fixed tissues
  • Ddx: neurotropic form of canine distemper, chronic wasting diseases like neoplasia, malabsorption, maldigestion, bacterial enteritis
86
Q

Aleutian disease - treatment, pathology

A
  • Disinfection with formalin, sodium hydroxide, phenolics
  • No general treatment, animals should be euthanized
  • Mink kits treated with gamma globulin-containing ADV antibody had decrease mortality rates
  • Necropsy: may have no lesions; infrequent hepatosplenomegaly & lymphadenopathy
  • Histo: periportal lymphocytic infiltrates; bile duct hyperplasia & periportal fibrosis; membranous glomerulonephritis
87
Q

Influenza in ferrets - etiology

A
  • Orthomyxovirus
  • Transmissible from humans to ferrets & ferrets to humans = vaccination of handlers, PPE, don’t work with ferrets if having respiratory illness
  • Human influenza viruses A & B pathogenic to ferrets (type B low pathogenicity)
  • Ferrets also susceptible to avian, phocine, equine, swine influenza - only swine causes clinical signs
88
Q

Influenza in ferrets - clin signs, epizootiology

A
  • Remains localized in nasal epithelium but may cause pneumonia
  • Clin signs = 48 hr postinfx; anorexia, fever, sneezing, serous nasal discharge, otitis
  • Secondary bacterial infection with Streptoccosu spp, Bordetella bronchiseptica
  • Transmission: aerosol, direct contact
89
Q

Influenza in ferrets - diagnosis, treatment, control

A
  • Recovery within 4 days (unlike CDV that progresses to death)
  • Dx: clinical signs & recovery within 4 days; hemagglutination inhibition antibody titers on acute and convalescent serum (rarely)
  • Tx: amantadine experimentally effective; neuraminidae inhibitors like zanamivir, oseltamivir - these prevent & treat influenza & may be used in combo with amantidin; antibiotics for secondary bacteria
  • Ferrets used as influenza model; used in influenza A research to study pathogenesis, Reye’s syndrome, evaluate vaccine trials
90
Q

Rabies in ferrets

A
  • Rhabdovirus, genus Lyssavirus
  • Experimental infection: mean incubation period of 28-33 days, mean morbidity was 4-5 days
  • Vaccinate with killed rabies vaccine at 3 mths, 1 year, then annually
  • Clin signs: anxiety, lethargy, posterior paresis
  • Pathology: Negri bodies may be seen in brain (not always), may be able to isolate virus from salivary glands
  • Suspect ferrets that bite or scratch humans = not less than 10 day quarantine for observation
  • Recent case report documented recovery and clearance of rabies virus in a ferret - survived for 100 days after onset of clinical signs with continued paraplegia
  • Dx: direct IFA of brain tissue
91
Q

Rotavirus in ferrets - etiology

A
  • Diarrhea in ferret kits - thought to be atypical poorly characterized rotavirus that has not been cultivated in vitro
  • Atypical rotaviruses lack the rotavirus common antigen
  • Definitive identification of a group C rotavirus in ferrets recently published
92
Q

Rotavirus in ferrets - epizootiology, transmission, clin signs

A
  • Diarrhea, perineal soiling
  • High mortality in young kits, lower mortality if over 10 days of age
  • May occur in kits as young as 1-4 days & up to 6 weeks of age
  • Secondary bacterial infection may increase severity of diarrhea
93
Q

Rotavirus in ferrets - pathology, diagnosis, treatment

A
  • Yellow-green liquid of mucous feces in terminal colon
  • Subtle small intestinal villous atrophy & epithelial cell vacuolation
  • Dx: electron microscopy of centrifuged fecal pellets; CANNOT use commercially available enzyme immunoassays
  • Tx: mortality reduced if kits continue nursing - syringe feed milk replacer; supportive care
  • Jills develop immunity to rotavirus infection & subsequent litters are protected
94
Q

Epizootic catarrhal enteritis in ferrets - etiology, transmission

A
  • A novel Alphacoronavirus = ferret enteric coronavirus (FRECV)
  • Occurs when young animal introduced to a colony of adults. though susceptible animals can be infected at any age
  • Virions shed in feces and saliva; intermittent shedding possible long after resolution of clinical disease
  • Transmission: rapid infection by oral route
  • High morbidity, low mortality
  • Considered enzootic
95
Q

Epizootic catarrhal enteritis in ferrets - clin signs, diagnosis

A
  • Decreased appetite, weight loss, lethargy, diarrhea - green mucoid, vomiting, dehydration
  • If chronic, malabsorption can occur & feces become small, ovoid
  • Elevated liver enzymes & nonspecific hematologic abnormalities in some ferrets
  • Young ferrets have milder disease than older ferrets
  • Dx: intestinal biopsy & histopath with IHC; RT-PCR; electron microscopy; a serologic test exists but should be evaluated in context of clinical signs
96
Q

Epizootic catarrhal enteritis in ferrets - pathology, treatment

A
  • Enteritis with watery intestinal contents, enlarged mesenteric LNs
  • Histo: LYMPHOCYTIC ENTERITIS WITH VILLOUS ATROPHY & necrosis and vacuolzation of enterocyte tips; villous blunting and fusion
  • Lesion are in JEJUNUM & ILEUM
  • Tx: aggressive oral & systemic fluid therapy; antibiotics for secondary bacteria; metronidazole
  • Most detergents and disinfectants will kill environmental coronavirus
97
Q

Ferret systemic coronavirus - etiology, transmission, clin signs

A
  • Systemic granulomatous disase due to ferret systemic coronavirus (FRSCV)
  • Genus Alphacoronavirus - behaves similarly to FIP dry form
  • Typically affects animals under 1 year of age
  • Transmission: mechanism unknown, but likely ingestion
  • Clin signs: lethargy, decreased appetite, diarrhea, vomiting, weight loss; some animals have neuro signs of ataxia, paresis, tremor, head tilt, seizure
98
Q

Ferret systemic coronavirus - diagnosis, pathology, treatment

A
  • Histo: intralesional coronaviral nucleic acid; IHC using monoclonal antibody (FIPV3-70) will localize nucleic acid
  • RT-PCR capable of differentiating FRSCV & FRECV
  • Clin signs + hematology strongly suggestive - nonregenerative anemia, hyperglobulinemia, hypoalbuminemia, thrombocytopenia
  • Ddx: Aleutian disease - due to FRSCV polyclonal gammopathy
  • Radiography & endoscopy for palpated masses
  • Necropsy: enlarged mesenteric LNs; multiple tan coalescencing nodules on serosal surfaces & mesenteric vessels
  • Histo: lesions most common in liver, kidney, spleen, lung; severe pyogranulomatous inflammation often surrounding vessels that infiltrates and destroys affected parenchyma; brain = pyogranulomatous meningoencephalitis
  • Tx: supportive care incl. iron in anemic animals, vitamins, gastroprotectants, immunostimulatory antibiotics like doxycycline
  • Most animals die or are euthanized within weeks of diagnosis
99
Q

Bovine herpesvirus 1 in ferrets

A
  • Infectious bovine rhinotracheitis (IBR)
  • Isolated from liver, spleen, lung of clinically normal ferrets
  • Raw beef suspected as source of infection
  • In experimental infection of ferrets, IBR caused either no respiratory pathology OR acute suppurative pharyngitis
100
Q

Hepatitis E virus in ferrets

A
  • Isolated from 4 ferrets in the Netherlands
  • No overt signs of disease
  • Relevance to ferret health or zoonotic risk unknown
101
Q

Suid herpesvirus 1 in ferrets

A
  • Pseudorabies virus (PRV), Aujeszky’s disease
  • Consumption of raw pork by ferrets
  • Usually fatal in most species infected
102
Q

Coccidiosis in ferrets - etiology, clin signs

A
  • 3 species of Isospora and Eimeria reported in ferrets: Isospora laidlawi, Eimeria furonis, Eimeria ictidea
  • Transmission: ingestion of sporulated oocysts
  • Clin signs: usually subclinical; diarrhea, lethargy, dehydration; rectal prolapse; one case of biliary infestation with E. furonis
  • Clin signs more common in young newly acquired ferrets after a stressful event
103
Q

Coccidiosis in ferrets - diagnosis, treatment

A
  • Dx: fecal float, direct wet mount; infestation of biliary tract resulted in changes on serum chemistry
  • Pathology: jejunum & ileum - villous and epithelial thickening; parasitic cysts and microorganisms within epithelium; mild granulomatous inflammation in villar lamina propria
  • Ddx: GI foreign body; dietary indiscretion, nutritional, inflammatory, infectious, other systemic diseases - proliferative colitis, salmonellosis, giardiasis, rotavirus, campylobacteriosis, eosinophilic gastroenteritis
  • In biliary case: hepatomegaly, enlarged firm bile ducts, thickened gallbladder wall
  • Control: good husbandry; cleaning cages with strong ammonium hydroxide solution; heat treatment of surfaces and utensils
  • Tx: sulfadimethozine for 6 days; ponazuril (triazine coccidiocidal drug) for 10 days
  • As with dogs and cats, the complete elimination of a coccidial infection requires an immunocompetent host
104
Q

Cryptosporidiosis in ferrets - etiology, transmission, clin signs

A
  • Etiology: Cryptosporidium spp.
  • Class Sporozoa, Subclass Cocidia
  • Inhabits respiratory and intestinal epithelium of birds, reptiles, mammals. fish
  • Transmission: ingestion of sporulated oocysts in contaminated food, water; life cycle similar to other coccidian parasites; autoinfection characteristic of life cycle
  • Clin signs: subclinical in both immunocompetent & immunosuppressed ferrets reported; otherwise nonspecific clinical signs with death possible in 48-72 hr
105
Q

Cyrptosporidiosis in ferrets - diagnosis, pathology, treatment

A
  • Dx: sugar solution centrifugation or fecal sedimentation using formalin-ether or formalin-ethyl acetate; direct fecal smear with methanol or heat fixing & stained with acid-fast - oocysts small compared to other coccidia - spherical to ellipsoidal; acid-fast; oocyst residuum is seen as a refractive dot under phase-contrast
  • Pathology: spherical to ovoid 2-5 um diameter organisms associated with brush border of villi; mild eosinophilic infiltrate in lamina propria of small intestine; ILEUM MOST COMMON HEAVILY INFECTED SECTION of small intestine
  • Tx: no known definitive treatment; supportive/symptomatic care; infections self-limiting in immunocompetent
  • ZOONOTIC
  • Drying, freeze-thawing, and steam cleaning inactivate the organism; few effective commercial disinfectants
106
Q

Sarcoptic mange in ferrets

A
  • Sarcoptes scabiei
  • Transmission: direct contact with infected hosts or fomites
  • Ferrets have Generalized or Pedal Form
  • Generalized: lesions are focal or generalized alopecia with intense pruritis
  • Pedal: lesions confined to toes and feet; feet become swollen with scabbing, nails may be deformed or lost
  • Dx: skin scraping or removing crusts, breaking them up, & clearing with 10& KOH for microscopic exam
  • Ddx: other pruritic external parasites like fleas; demodicois causes mild pruritis and alopecia in ferrets
  • Tx: Pedal = trim claws, remove scabs after softening in warm water; ivermectin SC or selamectin or lime sulfur dips; shampoos or soaks to reduce pruritis; antibiotics for secondary bacteria
107
Q

Demodicosis in ferrets

A
  • Demodex spp.
  • Found in normal skin, not considered contagious; predisposing factors incl immunologic or genetic conditions
  • Clin signs: alopecia, pruritis, orange discoloration of skin behind ears or on ventral abdomen & accompanying seborrhea
  • Dx: deep skin scraping; skin biopsy may be needed in chronic cases with thickened skin
  • Pathology: mites with a short, blunted abdomen similar to Demodex criceti; epidermis hypertrophic, mild superficial orthokeratotic hyperkeratosis, mild perivascular & superficial mixed cellular infiltrate
  • Ddx: sarcoptic mange, fleas, primary/secondary bacterial dermatitis
  • Tx: amitraz dip; imidacloprid-moxidectin; ivemectin orally or topically; selamectin
108
Q

Ear mites in ferrets

A
  • Otodectes cynotis
  • Transmission: direct contact with infested animal; entire life cycle completed in 3 weeks
  • Clin signs: usually asymptomatic; head shaking, mild to severe pruritis with inflammation & excoriation; secondary otitis interna with ataxia, circling, torticollis, Horner’s syndrome; brownish-black waxy discharge
  • Dx: otoscopic exam, microscope evaluation of ear slides
  • Tx: topical treatments more efficacious than injectable; ivermectin; due to anatomic characteristics of ferret ear, instillation of drops into the ear canal is of very limited efficacy; selamectin; imidacloprid-moxidectin; can give medications partially in ear canal & partially at interscapular region
  • High doses of ivermectin (0.2 mL of 1% solution) administered to jills at 2-4 weeks gestation resulted in high rates of congenital defects
109
Q

Fleas in ferrets

A
  • Ctenocephalides species
  • Transmission: direct contact with another infested animal or flea-infested environment
  • Clin signs: asymptomatic; mild to intense pruritis and alopecia of dorsal thorax and neck
  • Dx: clin signs, identification of fleas or flea excrement
  • Ddx: sarcoptic mange, demodex
  • Tx: concurrent treatment of environment & all animals in household is essential; rotenone or pyrethrin powders or sprays; selamectin topical; imidacloprid topical
110
Q

Pneumocystis carinii in ferrets

A
  • Fungus
  • Inhabits lungs of many different species; recent transmission studies suggest these fungi are highly species specific
  • Clin signs: only seen in immunocompromized ferrets (such as induced using high dose steroids)
  • Pathology: interstitial pneumonitis with mononuclear cell infiltrates
  • Dx: cysts and trophozites are evident with Gomori methanamine-silver nitrate and Giemsa on bronchoalveolar lavage
  • Tx: trimethoprim-sulfamethoxazole probably controls but does NOT eliminate infection
111
Q

Mucormycosis in ferrets

A
  • Ferrets susceptible o secondary fungal infection of outer ear canal with Absidia corymbifera or Malassezia spp.
  • These fungi widespread in environment & will cause secondary fungal infection in ears of ferrets infested with Otodectes cynotis
  • Dx: impression of ear exudates
  • Tx: eradicate underlying mite infestation followed by oral and topical ketoconazole, miconazole and polymyxin B
112
Q

Dermatomycosis in ferrest

A
  • Microsporum canis & Trichophyton mentagrophytes
  • ZOONOTIC
  • Control infection with general disinfection and destruction of contaminated beddings
  • Clin signs: circumscribed areas of alopecia inflammation that begin as small papules & spread peripherally in a scaly inflamed ring
  • Dx: yellow-green fluorescence of M. canis under UV light; skin scrapings digested with 10% KOH
  • Tx: griseofulvin causes clinical remission but may not clear infx
113
Q

Cryptococcosis in ferrets

A
  • Cryptococcus neoformans, Cryptococcus gatti
  • Immune suppression might be a contributing factor
  • Cryptococcus is found in soil, bird droppings, and trees
  • Prognosis is guarded and treatment is usually difficult
  • Tx: itraconazole for 10 months resulted in a successful outcome for C. neoformans variety grubii isolated from an enlarged submandibular LN
114
Q

Other ectoparasites of ferrets

A
  • Hypoderma bovis: granulomatous masses in cervical region
  • Cuterebra larvae: subdermal cysts in subcutis of nec
  • Flesh fly: infestation reported in commercially reared mink and ferrets housed outdoors
  • Ticks: may be found on ferrets housed outdoors
115
Q

Heartworm in ferrets - etiology, epizootiology, transmission

A
  • Dirofilaria immitis - filarial parasite transmitted by mosquitos
  • Microfilaria ingested by mosquitos and, after 2 molts, become infective 3rd stage larvae - infected larvae deposited into skin when mosquitos feed - larvae find way into body and migrate SC to thorax and eventually heart
  • Primary reservoir of infection is dogs, but heartworm may be found in a variety of mammals
  • All species except wild & domestic canids, domestic felines, ferrets, and California sea lions are considered aberrant hosts
116
Q

Heartworm in ferrets - clin signs, dx, treatment

A
  • Weakness, lethargy, depression, dyspnea, cyanosis, anorexia, dehydration, cough, pale MMs; moist lung sounds, muffled heart sounds; pleural or abdominal effusion; caval syndrome, mild anemia, biliverdinuria - may be of increased diagnostic value for this condition in ferrets
  • Dx: clin signs, radiography/US, microfilaremia - not consistent, testing for heartworm antigen may be more useful
  • Pathology: cardiomegaly, pleural and/or abdominal fluid and pulmonary congestion; adult worms in R atrium, R ventricle, pulmonary artery, cranial & caudal vena cava; microfilaria in small & large vessels in lungs
  • Ddx: primary cardiac disease - DCM; other systemic or pulmonary diseases
  • Tx: Prevent with monthly oral ivermectin or topical selamectin year-round (0.006 mg/kg body weight monthly); treatment with thiacetarsemide (same precautions as dogs - antithromboic therapy, treatment for heart failure, strict cage confinement); ivermectin until clin sins & microfilaremia resolve; melarsomine NOT recommended d/t adverse reactions
117
Q

Other nematodes in ferrets

A

-Ferrets are susceptible to infection with: Toxascaris leonina; Toxocara cati; Ancylostoma spp.; Dipylidium caninum; Mesocestoides spp.;
Atriotaenia procyonis; Trichinella spiralis; Filaroides martis; and Spiroptera nasicola

118
Q

Pregnancy toxemia in ferrets - etiology

A
  • Most common in primiparous jills carrying large litters; an inadvertant fast in late pregnancy is sometimes indicated
  • At least 75% of jills carrying more than 8 kits will develop if subjected to 24 hr of food withdrawal
  • Any jill with 15 of more kits may develop because abdominal space inadequate for uterus & amount of food required
  • Abnormal energy metabolism with hyperlipiemia, hypoglycemia, ketosis, hepatic lipidosis, decreased T4 and T3 levels
  • Excessive mobilization of free fatty acids
119
Q

Pregnancy toxemia in ferrets - clin signs, diagnosis, pathology, treatment

A
  • Anorexia, lethargy, melena, dehydration, easily epilated hair
  • Ddx: dystocia, metritis, pyometra, septicemia, renal failure, Helicobacter mustelae-induced gastric ulcer
  • Dx: azotemia, hypocalcemia, hypoproteinemia, elevated liver enzymes, anemia
  • Pathology: tan or yellow discolored liver, gastric hemorrhage, gravid uterus
  • Tx: if jill within a day of delivery, C-section and intensive postop support - force feeding gruel of high quality cat food & ferret chow, IV fluids with glucose, supplemental heat’ perform C-section under isoflurane or sevoflurane b/c metabolism of injectable agents prolonged by hepatic dysfunction
  • Agalactia common after C-section - hand feed or cross foster kits
  • Develop toxemia before 40 days of gestation = fluids & nutritional support until C-section can be performed
  • Prevention: feed highly palatable diet with >20% fat and >35% crude protein, avoid stress & dietary changes
120
Q

Hyperestrogenism in ferrets - etiology, clin signs

A
  • Ferrets are induced ovulators and may remain in persistent estrus if they are not bred or if estrus is not terminated chemically or by OVH
  • Estrogen-indued anemia possible in jills that remain in estrus for more than 1 month
  • Hyperestrogenism causes bone marrow hypoplasia of all cell lines in half of ferrets in prolonged estrus
  • Clin signs: vulvar enlargement, bilaterally symmetric alopecia of tail and abdomen, weakness, anorexia, depression, lethargy, weight loss, bacterial infection, mucopurulent vaginal discharge
  • Initial neutrophilia & thrombocytosis then lymphopenia, thrombocytopenia, neutropenia, anemia
  • Anemia begins as normocytic normochromic & progresses to macrocytic hypochromic
  • Coagulopathy assoc w/ hepatic dysfunction, thrombocytopenia = bleeding, pallor, melena, petechiation or ecchymosis, subdural hematoma, hematomyelia
121
Q

Hyperestrogenism in ferrets - pathology, treatment

A
  • Tissue pallor, light tan to pale pink bone marrow, hemorrhage, bronchopneumonia, hyddrometra, pyometra, mucopurulent vaginitis
  • Histo: cystic endometrial hypoplasia, hemosiderosis, diminised splenic extramedullary hemtopoiesis, mild to moderate hepatic lipiosis
  • Tx: terminate estrus & supportive care with antibiotics, blood transfusion, B vitamins, nutritional support
  • Estrus may be terminated by injection of 50-100 IU HCG or 20 ug of GnRH, repeated 1 week later if needed; OVH
  • PCV 25% or greater - good prognosis; PCV 15-25% guarded & may need blood transfusion; PCV less than 15% - poor prognosis
  • Repeated administration of hCG may result in sensitization and anaphylaxis - incoordination, tremor, vomiting, diarrhea - reverse with diphenhydramine; GnRH is smaller molecule = anaphylaxis less likely, GnRH implant is available
  • Estrogen induced anemia can be avoided by OVH, use of vasectomized hovs, or pharmacologic termination of estrus initiated 10 days after estrus onset
122
Q

Hyperammonemia in ferrets

A
  • Administration of arginine-free diets to young ferrets fasted for 16 hr leads to hyperammonemia and encephalopathy within 2-3 hr
  • Exacerbation of signs may be achieved by challenging young ferrets with influenza virus and aspirin - constitutes a model of Reye’s syndrome in children
  • Clin signs: lethargy, aggressiveness; then prostration, coma, death
  • Presumably occurs because of inability of ferrets to produce adequate amounts of ornithine from non-arginine precursors - detoxificaton of ammonia is therefore compromised
  • Ferrets older than 18 mths are unaffected by arginine-free diets
123
Q

Zinc toxicosis in ferrets

A
  • Ferrets of all ages are susceptible
  • Leaching of zinc from steam-sterilize galvanized food and water bowls
  • Clin signs: pallor, posterior weakness, lethargy
  • Dx: elevated levels of zinc in kidney and liver
  • Pathology: kidneys enlarged, pale, soft; livers orange; gastric hemorrhage
  • Histo: glomerular collapse, tubular dilation, tubular proteinaceous debris, focal cortical fibrosis, hepatic periacinar infiltration, depresstion of erythroid series
  • Avoid galvanized materials
124
Q

Hypothyroidism in ferrets

A
  • Clin signs: obesity, lethargy, decreased activity, excessive sleeping
  • Dx: measure T4 levels using human recombinant TSH
  • Tx: oral levothyroxine every 12 hr
125
Q

Traumatic disorders in ferrets

A
  • Fighting: separate hobs at 12 weeks of age to avoid
  • Traumatic elbow luxation: common in ferrets; typically occurs when animal changes directions after getting a leg caught in cage flooring; open reduction should be used because closed reduction rarely successful = tranarticular pin for 4 weeks with leg splinted until after pin removal
126
Q

Iatrogenic disorders in ferrets

A
  • Hydronephrosis due to ureter ligation & ovarian remnants = both related to OVH surgery
  • Ovarian remnants assoc w/ estrus, vulvar enlargement, alopecia
127
Q

4 major categories of neoplasia in ferrets

A
  • Pancreatic islet cell tumors
  • Adrenocortical cell tumors
  • Lymphoma
  • Skin cancers
128
Q

Insulinoma in ferrets

A
  • Functional pancreatic islet cell tumors = most common neoplasm in ferrets
  • In ferrets as young as 2 years, typically later onset at 4-5 years
  • Clin signs: weight loss, vomiting, ataxia; weakness with posterior paresis or collapse, splenomegaly, lymphcytosis; signs often intermittent or episodic
  • Hypoglycemia caused by excess production of insulin in neoplastic Beta-cells may cause tremors, disorientation, seizures
  • Excessive salivation and pawing at mouth
  • Dx: presumptive based on clin signs + hypoglycemia (check after 4 hr fasting period) - fasting glucose below 60 mg/dL considered diagnostic; 60-85 mg/dL suspect; concurrent hyperinsulinemia, but insulin secretion in affected ferrets can be sporadic; histology can provide definitive diagnosis = proliferation of pancreatic Beta-cells; can have local recurrence or mets to LNs, mesentery, spleen, liver
  • Ddx: anorexia, starvation, hepatic disease, sepsis, nonpancreatic neoplasia
  • Tx: medical management with prednisone +/0 diazoxide along with frequent feeding of high-protein meals; surgery recommended for animals that are healthy enough
129
Q

Adrenal tumors in ferrets

A
  • Second most common type of neoplasia in ferrets
  • Generally diagnosed between 3-6 years of age
  • Clin signs: asymptomatic; weight loss, bilateral symmetrical alopecia +/- pruritis
  • Clin signs directly related to increase of sex steroids in the blood resulting in estrogen toxicity
  • Difference between this condition and typical Cushing presentation is the production in affected ferrets of a significant increased of sex steroids by the zona reticularis and NOT significant levels of cortisol from the zona fasciculata
  • Sex steroids that are usually elevated are estradiol, 17-hydroxyprogesterone, testosterone, androstenedione
  • Estrus-like vulva swelling in females; prostatic changes and cystitis in males
  • Ddx: ovarian remnant
  • Dx: palpation reveals cranial abdominal masses, US shows increased adrenal size; serum assay of sex hormones
  • Alopecia can be seasonally intermittent
  • Adrenal cortical hyperplasia is extremely common in aging ferrets, even those not showing clinical signs
  • Tx: medical management: monthly injection of Lupron (leuprolide acetate) = GnRH superagonist & stops production of LH and FSH - resistant to Lupron may develop over time; Deslorelin implants are treatment of choice; GnRH vaccine for prevention; melatonin - directly inhibits GnRH release; Ferretonin (melatonin implant); surgical exploration and removal of enlarged adrenals; ultrasound-guided alcohol injection into affect adrenal
  • Frequently a tumor of the right adrenal will invade into the vena cava = partial resection or removal of vena cava needed; collateral vessels will make up for vena cava; survivors need aggressive fluid therapy for 2-3 days post-op
  • Histo: well-differentiated cells with a granular or vacuolated cytoplasm; adrenal cell carcinomas are less commonly found than adenomas & are larger, more pleomorphic, more invasive; mets can occur but are rare
130
Q

Bilateral adrenalectomy in ferrets

A
  • It is possible to remove both adrenal glands at the same time without creating significant hormonal issues
  • Animals should be medicated with dexamethasone during postop recover, & oral prednisone for a few weeks after surgery
  • Supplementation with glucocorticoids sometimes needed is the gland remaining after unilateral adrenalectomy has been suppressed by the hyperactive one
131
Q

Lymphoma in ferrets - etiology, clinical signs

A
  • Seen in all ages; an aggressive form is often seen in juvenile ferrets (less than 2 years of age) - mediastinal mass if often found
  • Older ferrets (greaters than 2 years old) more likely to develop more indolent form - multicentric or GI lymphoma
  • Potential etiologies: a retrovirus distinct to FeLV; chronic immune stimulation d/t ADV or Helicobacter mustelae (seems responsible for a specific type of gastric B-cell lymphoma)
  • Clin signs: often chronic, nonspecific signs - weight loss, anorexia, lethargy, splenic or hepatic enlargement, cutaneous involvement; anemia, lymphopenia or lymphocytosis; atypical lymphocytes in circulation; hypercalcemia with T cell lymphoma; dyspnea with mediastinal mass; elevated liver values, azotemia
  • Dx: FNA of masses, radiographs or US; IHC of affected tissues to determine cell immunophenotype
132
Q

IHC for ferret lymphoma

A
  • Anti-CD3 = B cell lymphoma

- Anti-CD79a = T cell lymphoma

133
Q

Lymphoma in ferrets - pathology, treatment

A
  • Tan colored masses in lymph nodes, spleen, liver, other organs; diffuse involvement may cause enlargement of these organs or thickening of wall of stomach or intestines
  • Histo: neoplastic lymphocytes
  • Tx: surgery, chemotherapy, radiation; simplest form of chemotherapy is prednisolone/prednisone - will achieve partial or complete, short term remission
  • Chemotherapy may be less effective in ferrets receiving chronic immunosuppression; most chemo regimens are modified feline lymphoma protocols
  • The more rapidly progressive form seen in younger ferrets should likely be treated more aggressively than the indolent form seen in adults
  • Doxorubicin, and to a lesser extent vincristine, can cause severe tissue sloughing if there is extravasation
134
Q

Skin tumors in ferrets

A
  • Mast cells tumors are most common integumentary tumors in ferrets - occur anywhere on body with associated alopecia, crusty ulceration, pruritis; histo: well differentiated mast cells with metachromatic cytoplasmic granules - toluidine blue stain
  • Basal cell tumors: firm plaques or pedunculated nodules that are white or pink; may grow rapidly and ulcerate; most are benign; Ddx: squamous cell carcinoma, apocrine gland adenocarcinoma
  • Chordomas: not epithelial cell tumors, but often present as firm masses on tail, may ulcerate overlying skin; arise along axial skeleton from notochord remnants, slow-growing; generally do not reoccur after tail amputation; prognosis guarded for rare cervical region chordomas - mets documented
135
Q

Placental-umbilical entanglement in ferrets

A
  • Has been assoc w/ fine particle bedding, large litters, short kit-birth intervals
  • Jills may neglect to clean placentas, or kits may be born so rapidly there is not adequate time
  • Entangled kits may die d/t dehydration, hypothermia, hypoglycemia
  • Tx: dissection under a heat lamp or on a heated surface to free kits; cords should be cut as far away from umbilicus as possible
  • Parturition should be supervised, if possible, to avoid entanglement
136
Q

Congenital defects in ferrets

A
  • Neural tube defect
  • Gastrochisis
  • Cleft palate
  • Amelia
  • Corneal dermoids
  • Cataracts
  • Supernumerary incisors
  • Cystic or polycystic kidneys
  • Cystic genitourinary anomalies assoc w/ prostate, bladder, proximal urethra likely develop secondary to aberrant hormone secretion by adrenocortical tumors
  • Newborn ferrets normally born with closed orbital fissure and are prone to developing subpalpebral abscesses
137
Q

Cardiomyopathy in ferrets

A
  • Common in aging ferrets
  • Dilatative form most commonly diagnosed
  • Clin signs: lethargy, weight loss, anorexia; hypothermia, tachycardia, cyanosis, jugular distension, respiratory distress
  • Dx: heart murmur/muffled sounds; hepato- & splenomegaly; radiographs; ECG
  • Tx: supportive care, diuretics, inotropic drugs
  • Long term prognosis is guarded to poor
138
Q

Splenomegaly in ferrets

A
  • Common finding in ferrets
  • May be related to another disease (insulinoma, cardiomyopathy, adrenal tumor, lymphoma, splenic sequestration of erythrocytes with anesthesia) or of unknown significant
  • Histo: extramedullary hematopoiesis (EMH) - may be incidental or play role in chronic anemia that may respond to splenectomy = syndrome called hypersplenism
139
Q

Eosinophilic gastroenteritis in ferrets

A
  • Idiopathic disorder with peripheral eosinophilia of 10-35% (but may not be elevated peripherally), hypoalbuminemia, diffuse infiltration of GI tract with eosinophils
  • Incidence is variable
  • Clin signs: chronic weight loss, anorexia, diarrhea, vomiting
  • Eosinophilic granulomas in mesenteric LNs; sometimes lung or liver may be involved
  • Splendore-Hoeppli material in inflamed LNs (Giemsa stain) - this is usually associated with helminths, bacteria, fungi, foreign bodies
  • Tx: supportive care for enteritis; ivermectin and corticosteroids may be beneficial
140
Q

Megaesophagus in ferrets

A
  • Clin signs: weight loss, anorexia, difficulty eating, repeated regurgitation
  • Cause generally unknown
  • Prognosis is poor, despite efforts at supportive care
141
Q

Disseminated idiopathic myofasciitis in ferrets

A
  • Emerging ferret disease first described in 2003
  • Inflammation of muscle and surrounding tissue
  • Ferrets under 18 months most commonly affected
  • Clin signs: fever, lethargy, depression, paresis, inappetance; lumbosacral or hind limb pain
  • Progressive disability leads to euthanasia in most cases
  • PE: wasting, muscle atrophy, lymphadenopathy and splenomegaly
  • ALT may be elevated but CK is not; hypoproteinemia and hypoglobulinemia sometimes observed
  • Dx: muscle biopsy
  • Pathology: areas of pallor or white streaks in various muscle groups including esophagus, diaphragmm, both axial and appendicular skeletal muscle
  • Histo: muscle fiber strophy, neutrophilic to pyogranulomatous infiltrate within and around muscle fibers of smooth, cardiac, and skeletal muscle; *transmural and circumferential esophageal infiltrate along the length of the organ is characteristic
  • Tx: combination of prednisone, cyclophosphamide, chloramphenicol may be successful
142
Q

Subpleural histiocytosis/Pleural lipidosis/Lipid pneumonia in ferrets

A
  • Gray, yellow, or white small raised lesion on surface of lungs
  • Histo: superficial thickening of lung tissue with mononuclear cell infiltration and varying degrees of fibrosis, with or without cholesterol-like clefts
  • Etiology unknown; appears to be incidental lesion

Laboratory Animal Medicine Blue Book, 3rd Ed. (2015) (16 decks)

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